PubMed · 6465513
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P Schüller. 1984. [Anesthesia problems in severe obesity].. https://pubmed.ncbi.nlm.nih.gov/6465513/
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The dopamine D(2)-like receptor agonist quinpirole has been reported to lower blood pressure. This effect appears to be mediated via activation of presynaptic D(2)-like receptors inhibiting the stimulated neural norepinephrine release. The aim of the present study was to investigate the role of renal nerves and the renin-angiotensin system (RAS) in the blood pressure lowering effect of quinpirole. Therefore, clearance experiments using different doses of quinpirole (0.3 to 100 microg/kg/min) were performed in thiopental-anesthetized rats with intact kidneys (INN) or 5 to 7 days after bilateral renal denervation (DNX). The functional involvement of the RAS in the blood pressure lowering effect of quinpirole was determined in rats pretreated with a subpressor dose of angiotensin II (10 microg/kg/min) or in rats pretreated with the angiotensin II (AT(1)) receptor antagonist losartan, in a subdepressor dose (10 microg/kg/min). Quinpirole dose-dependently decreased mean arterial blood pressure (MAP) by up to 29%. This blood pressure lowering effect of quinpirole was observed at lower doses in DNX rats when compared with INN animals (ED(50): 0.98 microg/kg/min in DNX vs. 6.02 microg/kg/min in INN animals). Quinpirole in a dose of 3 microg/kg/min, which did not affect MAP in vehicle treated INN rats, significantly reduced MAP in rats with losartan pretreatment. In DNX rats pretreated with angiotensin II the MAP-response to the infusion of 3 microg/kg/min quinpirole was clearly attenuated in comparison with untreated DNX animals. Our data show that stimulation of dopamine D(2)-like receptors dose-dependently decreased blood pressure, which was potentiated by both interruption of the renal innervation and AT(1) receptor blockade, while exogenous ANG II restored the enhancement of the blood pressure response to quinpirole. We conclude that the increased vasodilatory effect of quinpirole after renal denervation might depend on a decreased activity of the RAS.
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Urocortin is an endogenous vasodilator peptide that is related to corticotrophin-releasing factor. We examined the haemodynamic effects of urocortin in thiobutabarbital-anaesthetized rats, via the triple-isotope microspheres technique. Urocortin (3 nmol/kg, i.v. bolus) reduced mean arterial pressure (-25 mm Hg) through a decrease in total peripheral resistance (-43%). This was associated with an increase in cardiac output (+24%) and vasodilatation of the following tissues: heart and stomach (approximately 300% of baseline); liver, intestine, caecum/colon, skeletal muscle and skin (approximately 200%); and testes (approximately 150%). Arterial conductances of the kidneys, spleen and brain were unaffected by urocortin. Neither the vehicle (0.9% NaCl) nor a low dose of urocortin (0.3 nmol/kg) altered any measurements. Therefore, urocortin causes generalized vasodilatation as follows: heart and stomach>liver, intestine, caecum/colon, skeletal muscle and skin>testes.